Our principle objective remains the elucidation of the physiological character, mechanisms, and implications of disorders of renal acidification. We continue to be interested in the metabolic pathogenesis of the experimental model of type 2 renal tubular acidosis (RTA) induced in patients with hereditary fructose intolerance (HFI); the basis of the extraordinarily large alkali requirement of infants and children with classic renal tubular acidosis and the specific questions therin of whether a) endogenous production of nonvolatile acid becomes supernormal in rapidly growing, previously stunted infants and children; b) gut wasting of base occurs in some children with RTA: the role of aldosterone deficiency in disorders of renal acidification, both in patients who have this disorder in combination with hyporeninemia and chronic renal disease and in patients with isolated aldosterone deficiency; the mechanisms by which patients with classic (type 1) distal RTA fail to lower their urinary pH to normal.